Case Report ual orientation beginning in his The patient, a 57-year-old right-

Case Report
The patient, a 57-year-old righthanded man, sustained his first
cerebral vascular accident in the
right middle cerebral artery region
at the age of 45, which resulted in
right-sided hemiparesis that
resolved completely within 3
months. He continued to run his
private business successfully while
living with his mother.
The patient lost his father in
early childhood. There was no evidence of an emotional or conduct
disorder during school years, and
the patient eventually obtained his
university degree. He continued to
manage his successful practice until
he sustained the second cerebral
vascular accident in the left middle
cerebral artery region at age 53.
The patient became aware of his
homosexual orientation in his early
teens and had several gay partners.
He suffered a major depressive episode at age 26 that resolved within
a few months. He also had a diagnosis of excessive harmful use of
alcohol, but there was no evidence
of dependence.
The patient started complaining
of his changed personality and heterosexual orientation 6 months
after his second stroke. At the same
time he complained of excessive
mood swings and changed interests. He became preoccupied with
photography and had a successful
photographic exhibition a year
after his second stroke. His sexual
orientation remained heterosexual 4
years following the second stroke,
and he preferred to describe himself as bisexual because of his previous homosexual orientation.
The mechanism by which a person
acquires his sexual orientation is
complex and ranges from pure psychological theories to more complex biological concepts. Our
patient was aware of his homosex-
ual orientation beginning in his
early teens. He always enjoyed his
gay relationships and had had at
some point a live-in partner. He
grew up with an absent father and
had a strong bond with his mother.
He went back to live with his
mother after separating from his
partner 4 years before his first
stroke. It is unlikely that his psychological reaction to his first
and/or second stroke could explain
his altered sexual orientation, and
his sexuality was accepted by his
social network and family members.
Taking into consideration the
interval between his first and
second stroke, it is likely that an
organic process within the left
middle cerebral artery region is the
cause of his altered sexual orientation.
The sexual needs of patients suffering from a brain injury are centered on hyper- and hyposexuality
rather than altered sexual orientation. The alteration of sexual orientation raises serious challenges to
patients and their care. It may be
essential to address the issue of
sexual orientation in assessing
patient needs following brain
injury in addition to other possible
behavioral changes that might be
Sudad Jawad, M.D., FRCPI,
Welsh Neuropsychiatry and
Brain Injury Service,
Whitchurch Hospital,
Cardiff, United Kingdom
Charlotte Sidebothams,
School of Medicine,
University College Cardiff,
United Kingdom
Ruford Sequira, M.B.B.S.
Mental Health Unit,
Whitchurch Hospital,
Cardiff, United Kingdom
Nahla Jamil, M.R.C.P.,
Gwent Health Care,
Newport, South Wales,
United Kingdom
1. Arnold AP: The garden of voice within:
the normal origin of sex difference in the
brain. Curr Opin Neurol 2003; 13:759 –
2. Baily JM, Pillar RC: Genetics of human
sexual orientation. Annu Rev Sex Res
1995; 6:126 –156
3. Wegesin DJ: A neuropsychological profile of homosexual and heterosexual men
and women. Arch Sex Behav 1998; 27:91–
Capgras Syndrome
Associated With Fahr’s
To the Editor: Capgras syndrome is
a specific misidentification syndrome in which the person
believes that another person, with
whom he or she has close emotional ties as well as ambivalence
at the same time, has been
replaced by an persecutory
imposter. Capgras syndrome has
been found in a number of neuropsychiatric conditions like Alzheimer’s disease, parkinsonism, vascular dementia, stroke, multiple
sclerosis, and schizophrenia-likepsychosis.1 Fahr’s disease is a
clinical entity with idiopathic
bilateral basal ganglia calcification
in the absence of any clinical or
biochemical abnormality. Up to
50% of idiopathic bilateral basal
ganglia calcification present with
neuropsychiatric manifestations,
which include auditory and visual
hallucinations, complex delusions,
and schizophrenia-like psychosis.2
We describe an association
between idiopathic bilateral basal
ganglia calcification and Capgras
syndrome, which has not been
reported earlier.
J Neuropsychiatry Clin Neurosci 21:3, Summer 2009
Case Report
A 30-year-old woman diagnosed
with paranoid schizophrenia for 6
years was maintaining well on
olanzapine, 15 mg/day, with
good compliance. She presented
with a 6-month history of misidentifying her husband as an
imposter with malice, suggestive
of Capgras syndrome. There was
no other associated psychopathology. A detailed physical and neurological examination suggested
bilateral pedal pitting edema and
positive left-sided palmomental
reflex, without any evidence of
cognitive impairment or movement disorder. A contrast-enhanced CT brain scan revealed
bilateral basal ganglia calcification, involving the pallidal region
(Figure 1). Laboratory tests
including hemogram, thyroid
function test, and serum calcium
were within normal limits. A neurologist, whose opinion was
sought in view of the CT findings,
CT Scan of the Brain Showing
Bilateral Hyperdense Lesions
in Basal Ganglia
suggested the calcification as idiopathic. The patient’s olanzapine
was increased to 25 mg/day for
the next 3 months; following this
the Capgras phenomenon
resolved. However, she developed
delusions of infidelity during follow-up, which resolved after
increasing olanzapine to 30
In Capgras syndrome there is a
disruption of facial recognition circuitry, resulting in facial misidentification.3 The structural and functional neuroimaging studies in
Capgras syndrome have localized
the involvement of the bilateral
parietal and posterior frontal
regions with more frequent
involvement of the nondominant
cerebral hemisphere.4 Till now, no
particular circuit involving basal
ganglia has been implicated in
Capgras syndrome, although hypodensity of lenticular nucleus has
been reported.5 The CT scan of our
patient revealed idiopathic bilateral
basal ganglia calcification involving
the pallidum. We hypothesize that,
in our case, basal ganglia calcification could have disrupted one of
the cortico-subcortical circuits,
which might have some contribution in facial processing systems.
Basal ganglia calcification leading
to disruption of the thalamo-cortico-striatal circuit has been
reported to manifest as schizophrenia-like psychosis. The isolated
Capgras phenomenon in our case
could be a part of the schizophrenia process resulting from the same
mechanism.6 A dysfunctional input
of basal ganglia to the prefrontal
cortex as seen in Capgras syndrome in parkinsonism7 could be a
third proposition.
Biswa Ranjan Mishra, M.B.B.S.,
M.D., D.P.M.
J Neuropsychiatry Clin Neurosci 21:3, Summer 2009
Ravi Prakash, M.B.B.S., D.P.M.
Psychiatry, Central Institute of
Psychiatry, Kanke, Ranchi,
Jharkhand, India
Baikuntha Nath Mishra,
M.B.B.S., M.D., D.P.M.
Psychiatry, SCB Medical College, Cuttack, Orissa, India
Samir Kumar Praharaj,
M.B.B.S., M.D., D.P.M.
Vinod Kumar Sinha, M.B.B.S.,
M.D., D.P.M.
Psychiatry, Central Institute of
Psychiatry, Kanke, Ranchi,
Jharkhand, India
1. Feinberg TE, Roane DM: Delusional misidentification. Psychiatr Clin North Am
2005; 28:665– 683
2. Francis AF: Familial basal ganglia calcification and schizophreniform psychosis.
Br J Psychiatry 1979; 79:360 –362
3. Papageorgiou C, Lykouras L, Ventouras
E, et al: Abnormal P300 in a case of delusional misidentification with coinciding
capgras and Fre´goli symptoms. Prog
Neuropsychopharmacol Biol Psychiatry
2002; 26:805– 810
4. Eren I, Civi I, Yildiz M: Frontoparietal
hypoperfusion in capgras syndrome: a
case report and review. Turk Psikiyatri
Derg 2005; 16:284 –290
5. Paille`re-Martinot ML, Dao-Castellana
MH, Masure MC, et al: Frontoparietal
hypoperfusion in capgras syndrome: a
case report and review. Psychopathology
1994; 27:200 –210
6. Chabot B, Roulland C, Dollfus S: Schizophrenia and familial idiopathic basal
ganglia calcification: a case report. Psychol Med 2001; 31:741–747
7. Roane DM, Rogers JD, Robinson JH, et
al: Delusional misidentification in association with parkinsonism. J Neuropsychiatr Clin Neurosci 1998; 10:194 –198
Self-Induced “Therapeutic
Seizures” for the Treatment
of Depression
To the Editor: Early 20th century
research postulated an antagonism
between epilepsy and psychosis,